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Prenatal cadmium exposure impairs neural tube closure via inducing excessive apoptosis in neuroepithelium

Journal of Environmental Sciences 2024年第4期138卷 572-584页

作者： Shiyong Zhu Xuenan Li Xueyan Dai Jinlong Li College of Veterinary Medicine Northeast Agricultural UniversityHarbin 150030China key laboratory of the Provincial education department of heilongjiang for common animal disease prevention and treatment Northeast Agricultural UniversityHarbin 150030China heilongjiang key laboratory for laboratory animals and Comparative Medicine Northeast Agricultural UniversityHarbin 150030China

Birth defects have become a public health concern.The hazardous environmental factors exposure to embryos could increase the risk of birth defects.Cadmium,a toxic environmental factor,can cross the placental barrier during pregnancy.Pregnant woman may be subjected to cadmium before taking precautionary protective actions.However,the link between birth defects and cadmium remains obscure.Cadmium exposure can induce excessive apoptosis in neuroepithelium during embryonic development progresses.Cadmium exposure activated the p53 via enhancing the adenosine 5‘-monophosphate(AMP)-activated protein kinase(AMPK)and reactive oxygen species'(ROS)level.And cadmium decreases the level of Paired box 3(Pax3)and murine double minute 2(Mdm2),disrupting the process of p53 ubiquitylation.And p53 accumulation induced excessive apoptosis in neuroepithelium during embryonic development progresses.Excessive apoptosis led to the failure of neural tube closure.The study emphasizes that environmental materials may increase the health risk for embryos.Cadmium caused the failure of neural tube closure during early embryotic day.Pregnant women may be exposed by cadmium before taking precautionary protective actions,because of cadmium concentration-containing foods and environmental tobacco smoking.This suggests that prenatal cadmium exposure is a threatening risk factor for birth defects.

关键词： Cadmium Neural tube closure Excessive apoptosis p53 Embryogenesis

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Acetyl-11-keto-beta-boswellic acid promotes sciatic nerve repair after injury: molecular mechanism

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Neural Regeneration Research 2022年第12期17卷 2778-2784页

作者： Yao Wang Zong-Liang Xiong Xiang-Lin Ma Chong Zhou Mo-Han Huo Xiao-Wen Jiang Wen-Hui Yu department of Veterinary Medicine Northeast Agricultural UniversityHarbinHeilongjiang ProvinceChina College of Life Sciences Northeast Agricultural UniversityHarbinHeilongjiang ProvinceChina Key Laboratory of Heilongjiang Education Department for Common Animal Disease Prevention and Treatment Northeast Agricultural UniversityHarbinHeilongjiang ProvinceChina Institute of Chinese Veterinary Medicine Northeast Agricultural UniversityHarbinHeilongjiang ProvinceChina

Previous studies showed that acetyl-11-keto-beta-boswellic acid(AKBA),the active ingredient in the natural Chinese medicine Boswellia,can stimulate sciatic nerve injury repair via promoting Schwann cell proliferation.However,the underlying molecular mechanism remains poorly understood.In this study,we performed genomic sequencing in a rat model of sciatic nerve crush injury after gastric AKBA administration for 30 days.We found that the phagosome pathway was related to AKBA treatment,and brain-derived neurotrophic factor expression in the neurotrophic factor signaling pathway was also highly up-regulated.We further investigated gene and protein expression changes in the phagosome pathway and neurotrophic factor signaling pathway.Myeloperoxidase expression in the phagosome pathway was markedly decreased,and brain-derived neurotrophic factor,nerve growth factor,and nerve growth factor receptor expression levels in the neurotrophic factor signaling pathway were greatly increased.Additionally,expression levels of the inflammatory factors CD68,interleukin-1β,pro-interleukin-1β,and tumor necrosis factor-αwere also decreased.Myelin basic protein-andβ3-tubulin-positive expression as well as the axon diameter-to-total nerve diameter ratio in the injured sciatic nerve were also increased.These findings suggest that,at the molecular level,AKBA can increase neurotrophic factor expression through inhibiting myeloperoxidase expression and reducing inflammatory reactions,which could promote myelin sheath and axon regeneration in the injured sciatic nerve.

关键词： AKBA axon genomics inflammatory injury and repair myelin sheath myeloperoxidase neurotrophic factor peripheral nerve phagosome pathway regeneration Sprague-Dawley rat

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Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

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animal Nutrition 2021年第4期7卷 997-1008页

作者： Yingying Zheng Haoyue Guan Jie Yang Jingzeng Cai Qi Liu Ziwei Zhang College of Veterinary Medicine Northeast Agricultural UniversityHarbinChina College of animal Science and Veterinary Medicine Southwest Minzu UniversityChengduSichuanChina key laboratory of the Provincial education Department of Heilongjiang for Common Animal Disease Prevention and TreatmentCollege of Veterinary MedicineNortheast Agricultural UniversityHarbinChina

Selenium(Se)deficiency can seriously affect the small intestine of swine,and cause diarrhea in swine.However,the specific mechanism of Se deficiency-induced swine diarrhea has rarely been reported.Here,to explore the damage of Se deficiency on the calcium homeostasis and autophagy mechanism of swine,in vivo and in vitro models of swine intestinal Se deficiency were established.Twenty-four pure line castrated male Yorkshire pigs(45 d old,12.50±1.32 kg,12 full-sibling pairs)were divided into 2 equal groups and fed Se-deficient diet(0.007 mg Se/kg)as the Se-deficiency group,or fed Se-adequate diet(0.3 mg Se/kg)as the control group for 16 weeks.The intestinal porcine enterocyte cell line(IPEC-J2)was divided into 2 groups,and cultured by Se-deficient medium as the Se-deficient group,or cultured by normal medium as the control group.Morphological observations showed that compared with the control group,intestinal cells in the Se-deficiency group were significantly damaged,and autophagosomes increased.Autophagy staining and cytoplasmic calcium staining results showed that in the Sedeficiency group,autophagy increased and calcium homeostasis was destroyed.According to the reactive oxygen species(ROS)staining results,the percentage of ROS in the Se-deficiency group was higher than that in the control group in the in vitro model.Compared with the control group,the protein and mRNA expressions of autophagy-calcium-related genes including Beclin 1,microtubule-associated proteins 1 A(LC3-1),microtubule-associated proteins 1 B(LC3-2),autophagy-related protein 5(ATG5),autophagy-related protein 12(ATG12),autophagy-related protein 16(ATG16),mammalian target of rapamycin(mTOR),calmodulin-dependent protein kinase kinaseβ(CAMKK-β),adenosine 5’-monophosphate-activated protein kinase(AMPK),sarco(endo)plasmic reticulum Ca2+-ATPase(SERCA),and calpain in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro(P<0.05).Altogether,our results indicated that Se deficiency could destroy the calcium homeo

关键词： Se deficiency swine Small intestine Intestinal porcine enterocyte cell line Autophagy Ca overload

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Role of selenoprotein M knockdown in the melatonin antagonism of nickel-induced apoptosis and endoplasmic reticulum stress in mouse heart

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2023年第5期24卷 406-417页

作者： Xintong ZHANG Xiaoxue GAI Lihua XU Wenxue MA Qiaohan LIU Bendong SHI Cheng FANG Jingzeng CAI Ziwei ZHANG College of Veterinary Medicine Northeast Agricultural UniversityHarbin 150030China Suihua Agricultural and Rural Bureau Suihua 152000China College of Veterinary Medicine Northeast Agricultural UniversityHarbin 150030China4.Key Laboratory of the Provincial EducationDepartment of Heilongjiang for Common Animal Disease Prevention and TreatmentNortheast Agricultural UniversityHarbin 150030China

The aim of this study was to investigate the role of selenoprotein M(SelM)in endoplasmic reticulum stress and apoptosis in nickel-exposed mouse hearts and to explore the detoxifying effects of melatonin.At 21 d after intraperitoneal injection of nickel chloride(NiCl_(2))and/or melatonin into male wild-type(WT)and SelM knockout(KO)C57BL/6J mice,NiCl_(2)was found to induce changes in the microstructure and ultrastructure of the hearts of both WT and SelM KO mice,which were caused by oxidative stress,endoplasmic reticulum stress,and apoptosis,as evidenced by decreases in malondialdehyde(MDA)content and total antioxidant capacity(T-AOC)activity.Changes in the messenger RNA(mRNA)and protein expression of genes related to endoplasmic reticulum stress(activating transcription factor 4(ATF4),inositol-requiring protein 1(IRE1),c-Jun N-terminal kinase(JNK),and C/EBP homologous protein(CHOP))and apoptosis(B-cell lymphoma-2(Bcl-2),Bcl-2-associated X protein(Bax),Caspase-3,Caspase-9,and Caspase-12)were also observed.Notably,the observed damage was worse in SelM KO mice.Furthermore,melatonin alleviated the heart injury caused by NiCl_(2)in WT mice but could not exert a good protective effect in the heart of SelM KO mice.Overall,the findings suggested that the antioxidant capacity of SelM,as well as its modulation of endoplasmic reticulum stress and apoptosis,plays important roles in nickel-induced heart injury.

关键词： Selenoprotein M(SelM) Nickel chloride(NiCl_(2)) Melatonin Apoptosis Mouse heart

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Nano-selenium alleviates cadmium-induced cerebellar injury by activating metal regulatory transcription factor 1 mediated metal response

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animal Nutrition 2022年第4期11卷 402-412页

作者： Shao-Shuai Bi Milton Talukder Hai-Tao Jin Mei-Wei Lv Jing Ge Cong Zhang Jin-Long Li College of Veterinary Medicine Northeast Agricultural UniversityHarbin 150030China College of Biotechnology and Pharmaceutical Engineering of West Anhui University Lu’an 237012China department of Physiology and Pharmacology Faculty of Animal Science and Veterinary MedicinePatuakhali Science and Technology UniversityBarishal8210Bangladesh Quality and Safety Institute of Agricultural Products Heilongjiang Academy of Agricultural SciencesHarbin 150010China College of Veterinary Medicine Henan Agricultural UniversityZhengzhou 450002China key laboratory of the Provincial education department of heilongjiang for common animal disease prevention and treatment Northeast Agricultural UniversityHarbin 150030China heilongjiang key laboratory for laboratory animals and Comparative Medicine Northeast Agricultural UniversityHarbin 150030China

This study aims to investigate the role of metal regulatory transcription factor 1(MTF1)-mediated metal response in cadmium(Cd)-induced cerebellar injury,and to evaluate the antagonistic effects of nanoselenium(Nano-Se)against Cd toxicity.A total of 80 chicks(1 d old,male,Hy-Line Variety White)were randomly allocated to 4 treatment groups for 3 months:the control group(fed with a basic diet,n=20),the Nano-Se group(basic diet with 1 mg/kg nano-Se 1 mg/kg Nano-Se in basic diet,n=20),the NanoSe+Cd group(basic diet with 1 mg/kg Nano-Se and 140 mg/kg Cd Cl_(2),n=20)and the Cd group(basic diet with 140 mg/kg Cd Cl_(2),n=20).The results of the experiment showed that the Purkinje cells were significantly decreased with their degradation and indistinct nucleoli after Cd exposure.Moreover,exposure to Cd caused a significant accumulation of Cd and cupper.However,the contents of Se,iron,and zinc were decreased,thereby disturbing the metal homeostasis in the cerebellum.The Cd exposure also resulted in high levels of malondialdehyde(MDA)and down regulation of selenoprotein transcriptome.Furthermore,the expressions of MTF1,metallothionein 1(MT1),MT2,zinc transporter 3(ZNT3),ZNT5,ZNT10,zrt,irt-like protein 8(ZIP8),ZIP10,transferrin(TF),ferroportin 1(FPN1),ATPase copper transporting beta(ATP7B),and copper uptake protein 1(CTR1)were inhibited by Cd exposure.However,all these changes were significantly alleviated by the supplementation of Nano-Se.This study proved that Cd could disorder metal homeostasis and induce oxidative stress,whereas Nano-Se could relieve all these negative effects caused by Cd via activating the MTF1-mediated metal response in the cerebellum of chicken.

关键词： Nano-selenium Cadmium Selenoprotein transcriptome MTF1-mediated metal response Cerebellar injury

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Mechanisms by which microbial enzymes degrade four mycotoxins and application in animal production:A review

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animal Nutrition 2023年第4期15卷 256-274页

作者： Huiying Sun Ziqi He Dongwei Xiong Miao Long key laboratory of Livestock Infectious diseases Ministry of EducationKey Laboratory of Ruminant Infectious Disease Prevention and Control(East)Ministry of Agriculture and Rural AffairsChina College of animal Science and Veterinary Medicine Shenyang Agricultural UniversityShenyang110866China

Mycotoxins are toxic compounds that pose a serious threat to animal health and food safety.Therefore,there is an urgent need for safe and efficient methods of detoxifying mycotoxins.As biotechnology has continued to develop,methods involving biological enzymes have shown great promise.Biological enzymatic methods,which can fundamentally destroy the structures of mycotoxins and produce degradation products whose toxicity is greatly reduced,are generally more specific,efficient,and environmentally friendly.Mycotoxin-degrading enzymes can thus facilitate the safe and effective detoxification of mycotoxins which gives them a huge advantage over other methods.This article summarizes the newly discovered degrading enzymes that can degrade four common mycotoxins(aflatoxins,zearalenone,deoxynivalenol,and ochratoxin A)in the past five years,and reveals the degradation mechanism of degrading enzymes on four mycotoxins,as well as their positive effects on animal production.This review will provide a theoretical basis for the safe treatment of mycotoxins by using biological enzyme technology.

关键词： Mechanism Microbial enzyme Degradation Mycotoxin

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Effects of Matrine on Bovine Papilloma Virus-infected C127 Cells

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Journal of Northeast Agricultural University(English Edition) 2017年第2期24卷 51-58页

作者： Jiang Xiao-wen Liu Lin Feng Xin-xin Liu Yan-yan Chen Xue-ying Feng Guo-feng Song Jian-chen Li Yan-hua Yu Wen-hui College of Veterinary Medicine Northeast Agricultural University Harbin 150030 China department of Veterinary Medicine Yanbian University Yanji 133002 Jilin China heilongjiang key laboratory for animal disease Control and Pharmaceutical Development Harbin 150030 China

The aim of this study was to select drugs for prevention and treatment of bovine papilloma in vitro, using bovine papilloma virus（BPV-2） infected mouse mammary epithelial（C127） cell lines as the infectious cell model system. C127 cell shapes changed with BPV infection observed under light microscopy. C127 cell shapes changed with BPV infection observed under light microscopy. PCR was used to confirm BPV infected C127 cells. mR NA levels of matrine to BPV-2 infected C127 cells were detected by RT-PCR. Apoptosis of BPV-infected C127 cells treated with matrine was analyzed by flow cytometry. Results showed that 80 μg · mL-1 matrine had a direct virucidal and intervention effect of BPV-2. Matrine inhibited the proliferation of BPV-infected cells. Therefore, matrine might be regarded as a therapeutic drug candidate for BPV induced bovine papilloma disease treatment in future.

关键词： bovine papilloma virus C 127 cells matrine apoptosis

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Celastrol enhances transcription factor EB (TFEB)-mediated autophagy and mitigates Tau pathology:Implications for Alzheimer's disease therapy

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Acta Pharmaceutica Sinica B 2022年第4期12卷 1707-1722页

作者： Chuanbin Yang Chengfu Su Ashok Iyaswamy Senthil Kumar Krishnamoorthi Zhou Zhu Sichang Yang Benjamin Chunkit Tong Jia Liu Sravan G.Sreenivasmurthy Xinjie Guan Yuxuan Kan Aston Jiaxi Wu Alexis Shiying Huang Jieqiong Tan Kingho Cheung Juxian Song Min Li Mr.&Mrs.Ko Chi-Ming Centre for Parkinson’s disease Research School of Chinese MedicineHong Kong Baptist UniversityHong Kong SARChina department of Geriatrics Shenzhen People’s Hospital(the Second Clinical Medical CollegeJinan Universitythe First Affiliated HospitalSouthern University of Science and Technology)Shenzhen 518020China Institute for Research and Continuing education Hong Kong Baptist UniversityShenzhen 518057China College of Pharmacy Henan University of Chinese MedicineZhengzhou 450000China Center for Medical Genetics and Hunan key laboratory of animal Model for Human diseases School of Life SciencesCentral South UniversityChangsha 410078China Medical College of Acupuncture-Moxibustion and Rehabilitation Guangzhou University of Chinese MedicineGuangzhou 510632China

Alzheimer's disease(AD),characterized by the accumulation of protein aggregates including phosphorylated Tau aggregates,is the most common neurodegenerative disorder with limited therapeutic agents.Autophagy plays a critical role in the degradation of phosphorylated Tau aggregates,and transcription factor EB(TFEB)is a master regulator of autophagy and lysosomal biogenesis.Thus,small-molecule autophagy enhancers targeting TFEB hold promise for AD therapy.Here,we found that celastrol,an active ingredient isolated from the root extracts of Tripterygium wilfordii(Lei Gong Teng in Chinese)enhanced TFEB-mediated autophagy and lysosomal biogenesis in vitro and in mouse brains.Importantly,celastrol reduced phosphorylated Tau aggregates and attenuated memory dysfunction and cognitive deficits in P301S Tau and 3xTg mice,two commonly used AD animal models.Mechanistical studies suggest that TFEB-mediated autophagy-lysosomal pathway is responsible for phosphorylated Tau degradation in response to celastrol.Overall,our findings indicate that Celastrol is a novel TFEB activator that promotes the degradation of phosphorylated Tau aggregates and improves memory in AD animal models.Therefore,Celastrol shows potential as a novel agent for the treatment and/or prevention of AD and other tauopathies.

关键词： TFEB Autophagy Lysosome biogenesis Alzheimer’s disease(AD) Tau Celastrol mTOR Therapeutic target

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18β-glycyrrhetinic acid regulates mitochondrial ribosomal protein L35-associated apoptosis signaling pathways to inhibit proliferation of gastric carcinoma cells

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World Journal of Gastroenterology 2022年第22期28卷 2437-2456页

作者： Ling Yuan Yi Yang Xia Li Xin Zhou Yu-Hua Du Wen-Jing Liu Lei Zhang Lei Yu Ting-Ting Ma Jia-Xin Li Yan Chen Yi Nan College of Pharmacy Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina Traditional Chinese Medicine College Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina key laboratory of Hui Ethnic Medicine Modernization of Ministry of education Ningxia Medical UniversityYinchuan 750004Ningxia Hui Autonomous RegionChina department of Infectious diseases The Fourth Hospital of Harbin Medical UniversityHarbin 150001Heilongjiang ProvinceChina

BACKGROUND Gastric carcinoma(GC)is a common gastrointestinal malignancy worldwide.Based on the cancer-related mortality,the current prevention and treatment strategies for GC still show poor clinical results.Therefore,it is important to find effective drug treatment targets.AIM To explore the mechanism by which 18β-glycyrrhetinic acid(18β-GRA)regulates mitochondrial ribosomal protein L35(MRPL35)related signal proteins to inhibit the proliferation of GC cells.METHODS Cell counting kit-8 assay was used to detect the effects of 18β-GRA on the survival rate of human normal gastric mucosal cell line GES-1 and the proliferation of GC cell lines MGC80-3 and BGC-823.The apoptosis and cell cycle were assessed by flow cytometry.Cell invasion and migration were evaluated by Transwell assay,and cell scratch test was used to detect cell migration.Furthermore,a tumor model was established by hypodermic injection of 2.5×106 BGC-823 cells at the selected positions of BALB/c nude mice to determine the effect of 18β-GRA on GC cell proliferation,and quantitative reverse transcription-polymerase chain reaction(qRT-PCR)was used to detect MRPL35 expression in the engrafted tumors in mice.We used the term tandem mass tag(TMT)labeling combined with liquid chromatography–tandem mass spectrometry to screen for differentially expressed proteins(DEPs)extracted from GC cells and control cells after 18β-GRA intervention.A detailed bioinformatics analysis of these DEPs was performed,including Gene Ontology annotation and enrichment analysis,Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis,and so on.Moreover,STRING database(https://***/)was used to predict proteinprotein interaction(PPI)relationships and Western blot was used to detect the expression of proteins of interest in GC cells.RESULTS The results indicated that 18β-GRA could inhibit the proliferation of GC cells in a dose-and timedependent manner.It could induce GC cell apoptosis and arrest the cell cycle at G0/G1 phase.The proportion of cells arrested at S phase dec

关键词： Gastric carcinoma 18β-glycyrrhetinic acid Mitochondrial ribosomal protein L35 Proliferation Invasion Apoptosis

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CACA Guidelines for Holistic Integrative Management of Breast Cancer

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Holistic Integrative Oncology 2022年第1期1卷 76-126页

作者： Jiong Wu Daiming Fan Zhimin Shao Binghe Xu Guosheng Ren Zefei Jiang Yongsheng Wang Feng Jin Jin Zhang Qingyuan Zhang Fei Ma Jinli Ma Zhonghua Wang Shusen Wang Xiaojia Wang Shu Wang Haibo Wang Tao Wang Xiang Wang Jing Wang Jia Wang Biyun Wang Li Fu Hongyuan Li Yehui Shi Lu Gan Yunjiang Liu Jian Liu Zhenzhen Liu Qiang Liu Qiang Sun Wenwu Cheng Keda Yu Zhongsheng Tong Xinhong Wu Chuangui Song Jianguo Zhang Jian Zhang Junjie Li Bin Li Man Li Huiping Li Wentao Yang Hongjian Yang Benlong Yang Hong Bu Juping Shen Zhenzhou Shen Yiding Chen Ceshi Chen Da Pang Zhimin Fan Ying Zheng Xiaoli Yu Guangyu Liu Xichun Hu Yiqun Ling Jinhai Tang Yongmei Yin Cuizhi Geng Peng Yuan Yajia Gu Cai Chang Xuchen Cao Yuan Sheng Yuanxi Huang Jian Huang Weijun Peng Xiaohua Zeng Yuntao Xie Ning Liao Committee of Breast Cancer Society,Chinese Anti-Cancer Association key laboratory of Breast Cancer in Shanghai Department of Breast SurgeryFudan University Shanghai Cancer CenterShanghai Medical College of Fudan UniversityShanghaiChina department of Oncology Shanghai Medical College of Fudan UniversityShanghaiChina department of Gastroenterology Beijing Chaoyang HospitalCapital Medical UniversityBeijingChina State key laboratory of Cancer Biology National Clinical Research Center for Digestive Diseases and Xijing Hospital of Digestive DiseasesFourth Military Medical UniversityXi’anChina National Cancer Center/Cancer Hospital Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina department of Endocrine and Breast Surgery The First Affliated Hospital of Chongqing Medical UniversityYuzhongChongqingChina Medicine-Oncology The Affliated Hospital of Military Medical Sciences(The 307th Hospital of Chinese People’s Liberation Army)BeijingChina Breast disease Center Shandong Cancer HospitalJinanChina department of Breast Surgery The First Affliated Hospital of China Medical UniversityShenyangChina The 3rd department of Breast Cancer China Tianjin Breast Cancer PreventionTreatment and Research CenterTianjin Medical University Cancer Institute and HospitalNational Clinical Research Center of CancerTianjinChina Harbin Medical University Cancer Hospital HarbinChina department of Radiation Oncology Fudan University Shanghai Cancer CenterShanghai Medical College of Fudan UniversityShanghaiChina Sun Yat-Sen University Cancer Center GuangzhouChina Zhejiang Cancer Hospital HangzhouChina Breast Center Peking University People’s HospitalBeijingChina department of Breast Center The Affliated Hospital of Qingdao UniversityShandongChina department of Oncology Fifth Medical Center of Chinese PLA General HospitalBeijingChina department of Breast Surgical Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina Departmen

Purpose:Breast cancer is now the most common malignant tumor worldwide.About one-fourth of female cancer patients all over the world sufer from breast cancer.And about one in six female cancer deaths worldwide is caused by breast cancer.In terms of absolute numbers of cases and deaths,China ranks frst in the world.The CACA Guidelines for Holistic Integrative Management of Breast Cancer were edited to help improve the diagnosis and comprehensive treatment in China.Methods:The Grading of Recommendations Assessment,Development and Evaluation(GRADE)was used to classify evidence and consensus.Results:The CACA Guidelines for Holistic Integrative Management of Breast Cancer include the epidemiology of breast cancer,breast cancer screening,breast cancer diagnosis,early breast cancer treatment,advanced breast cancer treatment,follow-up,rehabilitation,and traditional Chinese medicine treatment of breast cancer patients.Conclusion:We to standardize the diagnosis and treatment of breast cancer in China through the formulation of the CACA Guidelines.

关键词： Epidemiology of breast cancer Breast cancer screening Breast cancer diagnosis Early breast cancer treatment Advanced breast cancer treatment Traditional Chinese medicine treatment of breast cancer

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